ATR and neoplasm: We would argue that under conditions of persistent and robust signalling of the ATM‐Chk2 and ATR‐Chk1 DNA damage checkpoints that we report here, the tumour cells must remarkably adapt in order to proliferate and avoid cell cycle arrest (senescence) or cell death otherwise evoked by such checkpoint signalling (Bartek et al., 2007, 2012; Halazonetis et al., 2008).